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| 3. |
- Hellgren Kotaleski, Jeanette, et al.
(författare)
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Control of burst proportion and frequency range by drive-dependent modulation of adaptation
- 1999
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Ingår i: Neurocomputing. - 0925-2312 .- 1872-8286. ; 26-27, s. 185-191
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Tidskriftsartikel (refereegranskat)abstract
- Factors controlling burst proportion in oscillatory networks are analyzed. This question is motivated by the lamprey swimming motor pattern which, independently on burst frequency, is characterized by a constant burst proportion. We investigate the effect of active modulation of the relative influence of a slower and faster adaptation controlling the depolarized phase. Using Morris–Lecar oscillators, NMDA-dependent oscillations or a network of mutually excitatory neurons, it is shown that the burst proportion can be controlled by increasing what corresponds to adaptation. Oscillations occur over an extended range of background stimulation values, leading to a higher maximal frequency.
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| 6. |
- Tegner, J, et al.
(författare)
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Computer simulations of low voltage activated calcium channels in the lamprey spinal network
- 1996
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Konferensbidrag (refereegranskat)abstract
- Low-voltage-activated calcium channels in the lamprey locomotor network: simulation and experiment. J. Neurophysiol. 77: 1795–1812, 1997. To evaluate the role of low-voltage-activated (LVA) calcium channels in the lamprey spinal locomotor network, a previous computer simulation model has been extended to include LVA calcium channels. It is also of interest to explore the consequences of a LVA conductance for the electrical behavior of the single neuron. The LVA calcium channel was modeled with voltage-dependent activation and inactivation using the m 3 h form, following a Hodgkin-Huxley paradigm. Experimental data from lamprey neurons was used to provide parameter values of the single cell model. The presence of a LVA calcium conductance in the model could account for the occurrence of a rebound depolarization in the simulation model. The influence of holding potential on the occurrence of a rebound as well the latency at which it is elicited was investigated and compared with previous experiments. The probability of a rebound increased at a more depolarized holding potential and the latency was also reduced under these conditions. Furthermore, the effect of changing the holding potential and the reversal potential of the calcium dependent potassium conductance were tested to determine under which conditions several rebound spikes could be elicited after a single inhibitory pulse in the simulation model. A reduction of the slow afterhyperpolarization (sAHP) after the action potential reduced the tendency for a train of rebound spikes. The experimental effects of γ-aminobutyric acid-B(GABAB) receptor activation were simulated by reducing the maximal LVA calcium conductance. A reduced tendency for rebound firing and a slower rising phase with sinusoidal current stimulation was observed, in accordance with earlier experiments. The effect of reducing the slow afterhyperpolarization and reducing the LVA calcium current was tested experimentally in the lamprey spinal cord, during N-methyl-d-aspartate (NMDA)-induced fictive locomotion. The reduction of burst frequency was more pronounced with GABAB agonists than with apamin (inhibitor of K(Ca) current) when using high NMDA concentration (high burst frequency). The burst frequency increased after the addition of a LVA calcium current to the simulated segmental network, due to a faster recovery during the inhibitory phase as the activity switches between the sides. This result is consistent with earlier experimental findings because GABAB receptor agonists reduce the locomotor frequency. These results taken together suggest that the LVA calcium channels contribute to a larger degree with respect to the burst frequency regulation than the sAHP mechanism at higher burst frequencies. The range in which a regular burst pattern can be simulated is extended in the lower range by the addition of LVA calcium channels, which leads to more stable activity at low locomotor frequencies. We conclude that the present model can account for rebound firing and trains of rebound spikes in lamprey neurons. The effects of GABAB receptor activation on the network level is consistent with a reduction of the calcium current through LVA calcium channels even though GABAB receptor activation will affect the sAHP indirectly and also presynaptic inhibition.
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| 7. |
- Tegner, J, et al.
(författare)
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Interactive effects of the GABABergic modulation of calcium channels and calcium-dependent potassium channels in lamprey
- 1999
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Ingår i: Journal of neurophysiology. - : American Physiological Society. - 0022-3077 .- 1522-1598. ; 81:3, s. 1318-1329
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Tidskriftsartikel (refereegranskat)abstract
- Interactive effects of the GABABergic modulation of calcium channels and calcium-dependent potassium channels in lamprey. The GABAB-mediated modulation of spinal neurons in the lamprey is investigated in this study. Activation of GABAB receptors reduces calcium currents through both low- (LVA) and high-voltage activated (HVA) calcium channels, which subsequently results in the reduction of the calcium-dependent potassium (KCa) current. This in turn will reduce the peak amplitude of the afterhyperpolarization (AHP). We used the modulatory effects of GABAB receptor activation on N-methyl-d-aspartate (NMDA)-induced, TTX-resistant membrane potential oscillations as an experimental model in which to separate the effects of GABAB receptor activation on LVA calcium channels from that on KCachannels. We show experimentally and by using simulations that a direct effect on LVA calcium channels can account for the effects of GABAB receptor activation on intrinsic membrane potential oscillations to a larger extent than indirect effects mediated via KCa channels. Furthermore, by conducting experiments and simulations on intrinsic membrane potential oscillations, we find that KCa channels may be activated by calcium entering through LVA calcium channels, providing that the decay kinetics of the calcium that enters through LVA calcium channels is not as slow as the calcium entering via NMDA receptors. A combined experimental and computational analysis revealed that the LVA calcium current also contributes to neuronal firing properties.
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| 8. |
- Tegner, Jesper, et al.
(författare)
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Low-voltage-activated calcium channels in the lamprey locomotor network : Simulation and experiment
- 1997
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Ingår i: Journal of Neurophysiology. - : American Physiological Society. - 0022-3077 .- 1522-1598. ; 77:4, s. 1795-1812
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Tidskriftsartikel (refereegranskat)abstract
- To evaluate the role of low-voltage-activated (LVA) calcium channels in the lamprey spinal locomotor network, a previous computer simulation model has been extended to include LVA calcium channels. It is also of interest to explore the consequences of a LVA conductance for the electrical behavior of the single neuron. The LVA calcium channel was modeled with voltage-dependent activation and inactivation using the m(3)h form, following a Hodgkin-Huxley paradigm. Experimental data from lamprey neurons was used to provide parameter values of the single cell model. The presence of a LVA calcium conductance in the model could account for the occurrence of a rebound depolarization in the simulation model. The influence of holding potential on the occurrence of a rebound as well the latency at which it is elicited was investigated and compared with previous experiments. The probability of a rebound increased at a more depolarized holding potential and the latency was also reduced under these conditions. Furthermore, the effect of changing the holding potential and the reversal potential of the calcium dependent potassium conductance were tested to determine under which conditions several rebound spikes could be elicited after a single inhibitory pulse in the simulation model. A reduction of the slow afterhyperpolarization (sAHP) after the action potential reduced the tendency for a train of rebound spikes. The experimental effects of gamma-aminobutyric acid-B (GABA(B)) receptor activation were simulated by reducing the maximal LVA calcium conductance. A reduced tendency for rebound firing and a slower rising phase with sinusoidal current stimulation was observed, in accordance with earlier experiments. The effect of reducing the slow afterhyperpolarization and reducing the LVA calcium current was tested experimentally in the lamprey spinal cord, during N-methyl-D-aspartate (NMDA)-induced fictive locomotion. The reduction of burst frequency was more pronounced with GABA(B) agonists than with apamin (inhibitor of K-(Ca) current) when using high NMDA concentration (high burst frequency). The burst frequency increased after the addition of a LVA calcium current to the simulated segmental network, due to a faster recovery during the inhibitory phase as the activity switches between the sides. This result is consistent with earlier experimental findings because GABA(B) receptor agonists reduce the locomotor frequency. These results taken together suggest that the LVA calcium chancels contribute to a larger degree with respect to the burst frequency regulation than the sAHP mechanism at higher burst frequencies. The range in which a regular burst pattern can be simulated is extended in the lower range by the addition of LVA calcium channels, which leads to more stable activity at low locomotor frequencies. We conclude that the present model can account for rebound firing and trains of rebound spikes in lamprey neurons. The effects of GABA(B) receptor activation on the network level is consistent with a reduction of the calcium current through LVA calcium channels even though GABA(B) receptor activation will affect the sAHP indirectly and also presynaptic inhibition.
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| 9. |
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| 10. |
- Tegnér, J, et al.
(författare)
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The synaptic NMDA component desynchronizes neural bursters
- 1999
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Ingår i: Neurocomputing. - 0925-2312 .- 1872-8286. ; 26-27, s. 557-563
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Tidskriftsartikel (refereegranskat)abstract
- The influence of excitatory and inhibitory coupling on synchronization depends on the temporal dynamics of the synapse. Slow excitation is desynchronizing whereas fast excitation tends to synchronize neuronal firing. Excitation via glutamatergic synapses, however, activates both ionotropic AMPA/kainate and NMDA receptors. Here we analyze the role of the synaptic NMDA component. We show that slowly bursting neurons desynchronize when connected by symmetrical NMDA synapses whereas they tend to synchronize when coupled with symmetrical AMPA/kainate synapses. This suggests that the effect on synchronization of an excitatory synapse also depends on the relative proportion of NMDA and AMPA/kainate synapses.
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